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  • 1
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    AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-01-23
    Description: The innate immune system senses nucleic acids by germline-encoded pattern recognition receptors. RNA is sensed by Toll-like receptor members TLR3, TLR7 and TLR8, or by the RNA helicases RIG-I (also known as DDX58) and MDA-5 (IFIH1). Little is known about sensors for cytoplasmic DNA that trigger antiviral and/or inflammatory responses. The best characterized of these responses involves activation of the TANK-binding kinase (TBK1)-interferon regulatory factor 3 (IRF3) signalling axis to trigger transcriptional induction of type I interferon genes. A second, less well-defined pathway leads to the activation of an 'inflammasome' that, via caspase-1, controls the catalytic cleavage of the pro-forms of the cytokines IL1beta and IL18 (refs 6, 7). Using mouse and human cells, here we identify the PYHIN (pyrin and HIN domain-containing protein) family member absent in melanoma 2 (AIM2) as a receptor for cytosolic DNA, which regulates caspase-1. The HIN200 domain of AIM2 binds to DNA, whereas the pyrin domain (but not that of the other PYHIN family members) associates with the adaptor molecule ASC (apoptosis-associated speck-like protein containing a caspase activation and recruitment domain) to activate both NF-kappaB and caspase-1. Knockdown of Aim2 abrogates caspase-1 activation in response to cytoplasmic double-stranded DNA and the double-stranded DNA vaccinia virus. Collectively, these observations identify AIM2 as a new receptor for cytoplasmic DNA, which forms an inflammasome with the ligand and ASC to activate caspase-1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726264/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726264/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hornung, Veit -- Ablasser, Andrea -- Charrel-Dennis, Marie -- Bauernfeind, Franz -- Horvath, Gabor -- Caffrey, Daniel R -- Latz, Eicke -- Fitzgerald, Katherine A -- AI-065483/AI/NIAID NIH HHS/ -- AI-067497/AI/NIAID NIH HHS/ -- R01 AI067497/AI/NIAID NIH HHS/ -- R01 AI067497-03/AI/NIAID NIH HHS/ -- R01 AI067497-04/AI/NIAID NIH HHS/ -- R01 AI067497-05/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Mar 26;458(7237):514-8. doi: 10.1038/nature07725. Epub 2009 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. veit.hornung@uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19158675" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins ; Caspase 1/*metabolism ; Cell Death ; Cell Line ; Cytoskeletal Proteins/genetics/*metabolism ; Cytosol/*metabolism ; DNA/immunology/*metabolism ; DNA-Binding Proteins ; Enzyme Activation ; Humans ; Inflammation/enzymology/*metabolism/pathology ; Mice ; Nuclear Proteins/chemistry/genetics/*metabolism ; Poly dA-dT/immunology ; Protein Binding ; Vaccinia virus/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Immunology. Select inflammasome assembly (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caffrey, Daniel R -- Fitzgerald, Katherine A -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):420-1. doi: 10.1126/science.1222362.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539706" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*metabolism ; GTP-Binding Proteins/*metabolism ; Humans ; Inflammasomes/*metabolism ; Macrophages/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    A long noncoding RNA mediates both activation and repression of immune response genes (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-03
    Description: An inducible program of inflammatory gene expression is central to antimicrobial defenses. This response is controlled by a collaboration involving signal-dependent activation of transcription factors, transcriptional co-regulators, and chromatin-modifying factors. We have identified a long noncoding RNA (lncRNA) that acts as a key regulator of this inflammatory response. Pattern recognition receptors such as the Toll-like receptors induce the expression of numerous lncRNAs. One of these, lincRNA-Cox2, mediates both the activation and repression of distinct classes of immune genes. Transcriptional repression of target genes is dependent on interactions of lincRNA-Cox2 with heterogeneous nuclear ribonucleoprotein A/B and A2/B1. Collectively, these studies unveil a central role of lincRNA-Cox2 as a broad-acting regulatory component of the circuit that controls the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376668/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carpenter, Susan -- Aiello, Daniel -- Atianand, Maninjay K -- Ricci, Emiliano P -- Gandhi, Pallavi -- Hall, Lisa L -- Byron, Meg -- Monks, Brian -- Henry-Bezy, Meabh -- Lawrence, Jeanne B -- O'Neill, Luke A J -- Moore, Melissa J -- Caffrey, Daniel R -- Fitzgerald, Katherine A -- AI067497/AI/NIAID NIH HHS/ -- GM053234/GM/NIGMS NIH HHS/ -- R01 AI067497/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):789-92. doi: 10.1126/science.1240925. Epub 2013 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23907535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/metabolism ; Cyclooxygenase 2/genetics ; Cytokines/genetics/metabolism ; Cytosol/metabolism ; *Gene Expression Regulation ; Heterogeneous-Nuclear Ribonucleoproteins/metabolism ; Immunity, Innate/*genetics ; Inflammation/*genetics ; Macrophage Activation ; Macrophages/*immunology/*metabolism ; Mice ; Models, Immunological ; RNA Interference ; RNA, Long Noncoding/*genetics/metabolism ; Toll-Like Receptors/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Positive Selection Drives Preferred Segment Combinations during Influenza Virus Reassortment (2015)
    Oxford University Press
    Details
    Publication Date: 2015-05-30
    Description: Influenza A virus (IAV) has a segmented genome that allows for the exchange of genome segments between different strains. This reassortment accelerates evolution by breaking linkage, helping IAV cross species barriers to potentially create highly virulent strains. Challenges associated with monitoring the process of reassortment in molecular detail have limited our understanding of its evolutionary implications. We applied a novel deep sequencing approach with quantitative analysis to assess the in vitro temporal evolution of genomic reassortment in IAV. The combination of H1N1 and H3N2 strains reproducibly generated a new H1N2 strain with the hemagglutinin and nucleoprotein segments originating from H1N1 and the remaining six segments from H3N2. By deep sequencing the entire viral genome, we monitored the evolution of reassortment, quantifying the relative abundance of all IAV genome segments from the two parent strains over time and measuring the selection coefficients of the reassorting segments. Additionally, we observed several mutations coemerging with reassortment that were not found during passaging of pure parental IAV strains. Our results demonstrate how reassortment of the segmented genome can accelerate viral evolution in IAV, potentially enabled by the emergence of a small number of individual mutations.
    Print ISSN: 0737-4038
    Electronic ISSN: 1537-1719
    Topics: Biology
    Published by Oxford University Press
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  • 5
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    Wrapping up BLAST and other applications for use on Unix clusters (2003)
    Oxford University Press
    Details
    Publication Date: 2003-02-12
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 6
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    Improved database searches for orthologous sequences by conditioning on outgroup sequences (2002)
    Oxford University Press
    Details
    Publication Date: 2002-01-01
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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